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Nathan Goodyear

A role for ghrelin in the central regulation of feeding : Abstract : Nature - 0 views

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    ghrelin plays central role in positive energy balance.  Ghrelin is produced from stomach to increase appetite prior to eating and then decreases post meal to provide satiety.  In some, the post meal ghrelin remains elevated and thus overeating ensues.  Important point, is that low ghrelin has been shown to lead to insulin resistance.
Nathan Goodyear

Ghrelin-Induced Food Intake Is Mediated via the Orexin Pathway - 0 views

  • Ghrelin, a peptide produced in the stomach and hypothalamus, stimulates feeding and GH secretion
  • Centrally administered ghrelin exerts an orexigenic activity through the neuropeptide Y (NPY)
  • though ghrelin is predominantly produced in endocrine cells of the stomach (17, 18), it is also synthesized in the hypothalamic arcuate nucleus (1, 19), a critical region for feeding
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    ghrelin stimulates feeding through orexin signaling.
Nathan Goodyear

Circulating Ghrelin Levels Are Decreased in Human Obesity - 0 views

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    low ghrelin levels found in obese individuals (Pima Indians).  Low ghrelin was associated with an inverse increase in fat, insulin, and leptin. It has also been shown to be associated with an inverse increase in Testosterone.
Nathan Goodyear

Pleasure Eating Triggers Body's Reward System and May Stimulate Overeating - 0 views

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    Ghrelin plays a role in overeating.  This is not much of a surprise as Ghrelin has been shown to be a major appetite driver and has been linked to higher calorie intake of foods.
Nathan Goodyear

Short Sleep Duration Is Associated with Reduced Leptin, Elevated Ghrelin, and Increased... - 0 views

  • Participants with short sleep had reduced leptin and elevated ghrelin
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    poor sleep reduces leptin and elevates ghrelin.  This will contribute to weight gain.
Nathan Goodyear

Ghrelin, leptin, adiponectin, and insulin levels a... [Menopause. 2011] - PubMed - NCBI - 0 views

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    ghrelin, leptin, adiponectin, and insulin weave a complex web in obesity
Nathan Goodyear

Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia ... - 0 views

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    ghrelin resistance?  that is one suggested pathophysiologic mechanism in people with anorexia nervosa
Nathan Goodyear

Ghrelin Enhances Appetite and Increases Food Intake in Humans - 0 views

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    ghrelin stimulates appetite and thus food intake.  It also stimulates GH release
Nathan Goodyear

Ghrelin is a growth-hormone-releasing acylated peptide from stomach : Abstract : Nature - 0 views

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    ghrelin is a GH releasing peptide released from the stomach
Nathan Goodyear

A Preprandial Rise in Plasma Ghrelin Levels Suggests a Role in Meal Initiation in Humans - 0 views

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    pre-meal rise in ghrelin increases appetite and plays role in positive energy balance.
Nathan Goodyear

Influence of ghrelin on food ... [Curr Opin Clin Nutr Metab Care. 2007] - PubMed - NCBI - 0 views

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    Ghrelin is an orexin that increases energy intake i.e. increases food intake.
Nathan Goodyear

The role of leptin and ghrelin in the regulation o... [Obes Rev. 2007] - PubMed result - 0 views

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    leptin and ghrelin and how they manipulate what you eat.  Instead of focusing on what target to create to attack, how about how to balance them to create healthy eating habits
Nathan Goodyear

Plasma Ghrelin Levels after Diet-Induced Weight Loss or Gastric Bypass Surgery - NEJM - 0 views

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    "diets" and weight-loss surgery effect ghrelin diferently
Nathan Goodyear

Foods fail to suppress Ghrelin levels in obese humans - 0 views

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    Ghrelin is a hormone that is release to induce hunger and eating. Post meals, gherlin should decrease; but in obese individuals, a dysregulation between the GI system and the hypothalamus results in elevated gherlin resulting in overeating.
Nathan Goodyear

Metabolic influences on neuroendocrine regulation of reproduction - 0 views

  • Energy storage occurs mainly at the level of white adipose tissue, where adipocytes secrete the anorexigenic adipokine leptin
  • humans and laboratory animals with leptin or insulin deficiency or resistance and/or increased ghrelin levels exhibit delayed or absent puberty and frequently display hypogonadotropic hypogonadism, which prevents fertility
  • Ghrelin suppresses pulsatile gonadotropin-releasing hormone (GnRH) release [14,15], thus serving as a signal to suppress reproduction in times of famine
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  • GnRH neurons have been shown to express insulin receptor mRNA and protein [27] and are activated by insulin
  • AgRP and NPY have the opposite (orexigenic) effect, inducing food intake.
  • Neuropeptides derived from POMC/CART neurons exert a potent anorectic action, thus decreasing food intake and body weight
  • Kisspeptins (encoded by KISS1) have been identified in the last decade as the most potent secretagogues of GnRH release.
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    Good, although brief, discussion of the interaction between metabolism and hormones.  Kisspeptin is a GNRH secreatagogue "upstream".   Insulin, Leptin, and Gherlin can inhibit GNRH through resistance and low levels.  Probably a U shaped graph of optimal activity.
Nathan Goodyear

Weight Regain after a Diet-Induced Loss Is Predicted by Higher Baseline Leptin and Lowe... - 0 views

  • Appetite-related hormones may play an important role in weight regain after obesity therapy.
  • Subjects with higher plasma leptin and lower ghrelin levels at baseline could be more prone to regain lost weight
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    leptin plays role in rebound weight gain after "diet" programs
Nathan Goodyear

Obestatin partially affects ghrelin stimulatio... [Endocrinology. 2007] - PubMed - NCBI - 0 views

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    obestatin inhibits food intake and slow GI motility.  THis is the opposite of ghrelin, which increases appetite
Nathan Goodyear

Obesity - Resistin, Adiponectin, Ghrelin, Leptin, and Proinflammatory Cytokines: Relati... - 0 views

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    obesity is dynamically complex!
Nathan Goodyear

Testosterone, the male hormone connection: treating diabetes and heart disease. - 0 views

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    good, well referenced discussion of how Testosterone support for those with low T can improve Diabetes, insulin function, improve energy balance, and reduce cardiovascular disease risk. The discussion discusses many of the moving parts in how testosterone improves CVD risk.
Nathan Goodyear

ScienceDirect.com - Cell Metabolism - Estrogen Receptors and the Metabolic Network - 0 views

  • The pro-opiomelanocortin (POMC) neurons have an anorexigenic action and, when activated, reduce food intake through the release of two peptides, α-melanocyte-stimulating hormone (α-MSH) and cocaine-and-amphetamine-regulated transcripts (CART). The neuropeptide Y (NPY) neurons, on the other hand, release NPY hormone and agouti gene-related protein (AgRP), which prevent the binding of α-MSH to MC3R and MC4R, increasing food intake
  • This suggests that the central anorexic effects of E2 may occur via ERβ
  • The main hypothalamic areas involved in food intake and satiety are the arcuate nucleus (ARC), the lateral hypothalamus (LH), the paraventricular nucleus (PVN), the ventromedial hypothalamus (VMH), and the dorsomedial hypothalamus (DMH)
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  • Leptin is a potent anorexigenic and catabolic hormone secreted by adipose cells that reduces food intake and increases energy expenditure
  • E2 not only modulates leptin receptor mRNA in the ARC and VMH, but also increases hypothalamic sensitivity to leptin, altering peripheral fat distribution
  • ghrelin. It acts on growth hormone secretagogue receptors (GHSR1a) located in the ARC and is a potent stimulator of food intake
  • It thus appears that of the two ERs, ERα plays a predominant role in the CNS regulation of lipid and carbohydrate homeostasis.
  • Both ERs have been identified in the ARC
  • Stimulation of MCH neurons increases food intake and fat accumulation while its inhibition leads to decreased food intake and reduced fat accumulation.
  • Both ERs have been identified in the LH
  • both ERs have been identified in this nucleus
  • The PVN is the region of the hypothalamus with the highest expression of ERβ and is reported to be weakly ERα positive
  • The VMH is ERα regulated
  • Skeletal muscle is responsible for 75% of the insulin-induced glucose uptake in the body
  • GLUT4 is highly expressed in muscle and represents a rate-limiting step in the insulin-induced glucose uptake
  • data suggest that in the physiological range, E2 is beneficial for insulin sensitivity, whereas hypo- or hyperestrogenism is related to insulin resistance
  • In aging female rats, E2 treatment improves glucose homeostasis mainly through its ability to increase muscle GLUT4 content on the cell membrane
  • It is evident that ERα and ERβ have distinct actions and that much more research is needed to clearly identify the function of each receptor in muscle.
  • E2 prevents accumulation of visceral fat, increases central sensitivity to leptin, increases the expression of insulin receptors in adipocytes, and decreases the lipogenic activity of lipoprotein lipase in adipose tissue
  • In rats, ovariectomy increases body weight, intra-abdominal fat, fasting glucose and insulin levels, and insulin resistance followed by decreased phosphorylation of AMPK and its substrate acetyl-CoA carboxylase in adipose tissue
  • decreased adiponectin, PPARγ coactivator-1α (PGC-1α), and uncoupling protein 2 (UCP2) and increased resistin
  • Men with aromatase deficiency have truncal obesity, elevated blood lipids, and severe insulin resistance
  • Although not all studies are in agreement, polymorphisms of ERα in humans have been associated with risk factors for CVDs
  • Human subcutaneous and visceral adipose tissues express both ERα and ERβ, whereas only ERα mRNA has been identified in brown adipose tissue
  • suggesting that ERα is the main regulator of GLUT4 expression in adipose tissue
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    very nice article that looks at the balance of ER-alpha/ER-beta and their role in metabolic syndrome.  This article discusses the balance of  these receptors are tissue dependent in their effect.  I like their conclusion: "...but these mechanisms will never be completely understood if they are not considered in the context of a whole system.
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